Modeling intraspecific chemodiversity - theory and first results

Explaining the causes and effects of different types of diversity is one of the key research missions in ecology and evolutionary biology. Plants produce numerous metabolites. There is a great diversity of metabolites between species, populations, and members of the same population. This chemodiversity has numerous ecological and economic implications. However, the mechanisms which maintain chemodiversity are still largely unknown. A theoretical framework is needed as a first step to bridge this gap in evolutionary knowledge. The goal of this project is therefore to develop mathematical and computational models linking genes, enzymes, metabolites, and ecological interactions to start building a theoretical framework for the evolutionary emergence and maintenance of plant chemodiversity. The screening hypothesis postulates that plants developed a set of biosynthetic pathways in which a great number of metabolites can quickly evolve. The more metabolites there are, the more likely it is that some have a defensive role against herbivores. Additionally, in existing models for the maintenance of other types of diversity, different types of negative frequency-dependent-selection (NFDS) frequently play an important role. In this project, we develop models based on the screening hypothesis and NFDS to investigate whether these hypotheses can explain how observed chemodiversity may have evolved and may be maintained. We will work together closely with empiricists to produce models which can be used to predict possible and empirically testable evolutionary pathways for model species based on realistic assumptions about these species. In the first phase of the project, we develop an individual-based model of a plant population and implement it in C++. This model includes a submodel of the biosynthetic pathways which determine the metabolites each individual produces. In the pathway, a primary metabolite is modified by various enzymes. The coding and regulatory genes for these enzymes evolve through mutation, gene duplication, and gene loss. The resulting metabolite(s) determine the fitness effects of each individual genotype. On my poster, I will present the evolutionary thought behind the model and the results from the first phases of the implementation.